Various cardiac diseases exhibit cardiac arrhythmia. Different treatment options exist for treating the arrhythmia that may arise from these diseases. The most common treatment includes implantable cardiac defibrillators (ICD) and drug therapy. ICDs have been available in the United States since the mid-1980s and have a well-documented success rate in controlling cardiac arrhythmia caused by various heart diseases. An ICD has two basic components: the ICD generator and the lead system for pacing and shock delivery to which it is connected. An ICD generator contains sensing circuits, memory storage, capacitors, voltage enhancers, a telemetry module, and a control microprocessor. Advances in miniaturization and complexity in all of these components have permitted a tremendous reduction in size of the generator itself despite increased functionality, such as added programming options, anti-tachycardia pacing, single- and dual-chamber rate-responsive pacing for bradycardia, biphasic defibrillation waveforms, enhanced arrhythmia detection features, and innovations in lead systems.
Current ICD technology, however, provides for the detection and recognition of an arrhythmia based on the sensed heart rate once it has already started. Although there have been several attempts at developing new technology for predicting the onset of a cardiac arrhythmia, many of these methods and systems appear to rely primarily on events occurring within the heart, such as sensed heart rate and electrocardiography (ECG). For example, one method and device predict cardiac arrhythmias by gathering and processing electrocardiographic data, such as intervals between heart beats (RR-series) or other heart signals, to predict the occurrence of a cardiac arrhythmia. Another method and apparatus forecast arrhythmia based on real-time intact intracardiac electrograms.
In an effort to predict cardiac arrhythmias without reliance on events occurring within a heart, methods and devices have been disclosed that use elevated sympathetic nerve discharges in a patient for cardiac arrhythmia predictions. For example, in U.S. Pat. No. 7,266,410, the disclosed methods and systems generally comprise monitoring the sympathetic neural discharges of a patient from the stellate ganglia, the thoracic ganglia, and/or any other sympathetic nerve identified as having an influence over the heart rate of a patient. Other sympathetic nerves suitable for use in connection with the prediction of cardiac arrhythmias may be generally determined by obtaining simultaneous recordings of neural discharges and heart rate in a test subject and determining whether there exists a correlation between an observed increase in the amplitude and/or frequency of the neural discharges and an increase in heart rate.
Elevated stellate ganglia nerve activity (SGNA) has been demonstrated to precede the onset of cardiac arrhythmias. In one known system, the sympathetic neural discharges may be monitored by a sensor or electrode that is implanted in the stellate ganglia to measure the stellate ganglia nerve activity (SGNA) of the patient from the left stellate ganglion (LSG), the right stellate ganglion (RSG), or both. For example, the electrode may directly sense electrical activity of the stellate ganglia and transmit this data to a processor. The processor may then analyze the data acquired from the electrode and, upon the determination that the SGNA has increased beyond a defined normal value, produce an output signal indicating the likely onset of an arrhythmia, myocardial ischemia, and/or other diseased condition of the heart associated with elevated sympathetic nerve discharges. Another known system compares the parameters for the sensed and normal sympathetic neural discharges in the patient to detect an increase in the sympathetic neural discharge in a patient. An increase in sympathetic neural discharge may also be determined by detecting increases in the amplitude and frequency of the sensed sympathetic neural discharge beyond defined normal values, such as the sensed electrical activity of the stellate ganglia and/or the thoracic ganglia. Predictions of cardiac arrhythmia based on nerve activity from the stellate ganglia are thought to be especially reliable.
While these systems and methods are able to detect an increased likelihood of an occurrence of a cardiac arrhythmia, they do require the implantation of a sensor in the LSG or the RSG, or both. This implantation involves surgery in the vicinity of the spinal column, rather than the heart. Devices that treat cardiac arrhythmia by stimulating myocardial hyperinnervation in the sinus node and right ventricle of the heart of the patient are designed for use with electrodes that have been placed within, but not outside, of the heart. Similarly, devices that apply cardiac pacing, cardioversion, or defibrillation shocks, also use electrodes that are implanted in the heart. Using electrodes coupled to the heart to obtain nerve activity signals, however, is technically difficult because the heart is a strong electrical signal generator. Thus, the detection and monitoring of nerve activity in the noisy environment of the heart is difficult.